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Pathological mechanism
NameAbeta decreases dendritic spine number, causes dysmorphic spine shapes
Description
Hypothesis
Dendritic Spine Hypothesis show other
Extracelular pathological element
β-Amyloid show other
Intracelular pathological element
Pathological action
Reduces show other
Process
Dendritic spine density show other
Process action
Decreases show other
Transmitter(s)
Receptor(s)
Glutamate show other
Channel(s)
Pharmacological Agent
alpha7 nicotinic receptor antagonists show other
NMDA receptor blockers show other
Pharmacological Action
Blocks show other
Brain region
Neuron
Cell model
Cellular compartment
PubMed ID17368908
Citation
AlzWeb
NotesCalabrese, B., Shaked, G. M., Tabarean, I. V., Braga, J., Koo, E. H., & Halpain, S. (2007). Rapid, concurrent alterations in pre- and postsynaptic structure induced by naturally-secreted amyloid-beta protein. Molecular and Cellular Neurosciences, 35(2), 183-193. Within 1-2 h picomolar concentrations of cell-derived, soluble Abeta cause Clusters of presynaptic vesicle markers to decrease in size and number at glutamatergic but not GABAergic terminals. Dendritic spines also decreased in number and became dysmorphic, as spine heads collapsed and/or extended long protrusions. Simultaneous time-lapse imaging of axon-dendrite pairs revealed that shrinking spines sometimes became disconnected from their presynaptic varicosity. Concomitantly, miniature synaptic potentials decreased in amplitude and frequency. Spine changes were prevented by blockers of nAChRs and NMDARs. Washout of Abeta within the first day reversed these spine changes.
Pathology
Alzheimer show other
Stage
Early show other
Question
Claim
Loss/alteration of dendritic spines in early Alzheimer's show other

Other categories referring to "Abeta decreases dendritic spine number, causes dysmorphic spine shapes"

 
Revisions:3
Last time:11/21/2008 12:51:18 PM
Reviewer:Pradeep Mutalik
Owner:Pradeep Mutalik

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